This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. During the reporting period, we found that the cannibinoid receptor 1 antagonist blocks extinction of conditioned fear and that this can be reversed by a cholecystokinin receptor antagonist. This suggested that endocannabinoids normally inhibit release of cholecystokinin which can disrupt fear extinction. We found that cocaine increased the acoustic startle reflex in rhesus monkeys and that this effect did not slow tolerance after chronic cocaine administration. Olfactory fear conditioning led to an increase in the number of olfactory sensory neurons in the nasal epithelium and therefore increased olfactory sensory axons into the olfactory bulb. Additionally, we found that neuropeptide Y in the amygdala can facilitate fear extinction.